Protein Corona-Directed Cellular Recognition and Uptake of Polyethylene Nanoplastics by Macrophages.

The widespread use of plastic products in daily life has raised concerns about the health hazards associated with nanoplastics (NPs). When exposed, NPs are likely to infiltrate the bloodstream, interact with plasma proteins, and trigger macrophage recognition and clearance. In this study, we focused on establishing a correlation between the unique protein coronal signatures of high-density (HDPE) and low-density (LDPE) polyethylene (PE) NPs with their ultimate impact on macrophage recognition and cytotoxicity. We observed that low-density and high-density lipoprotein receptors (LDLR and SR-B1), facilitated by apolipoproteins, played an essential role in PE-NP recognition. Consequently, PE-NPs activated the caspase-3/GSDME pathway and ultimately led to pyroptosis. Advanced imaging techniques, including label-free scattered light confocal imaging and cryo-soft X-ray transmission microscopy with 3D-tomographic reconstruction (nano-CT), provided powerful insights into visualizing NPs-cell interactions. These findings underscore the potential risks of NPs to macrophages and introduce analytical methods for studying the behavior of NPs in biological systems.

Silver Nanoparticles Induce Apoptosis in HepG2 Cells through Particle-Specific Effects on Mitochondria.

Silver nanoparticles (AgNPs) have been widely used in biomedical and consumer products. It remains challenging to distinguish the toxicity of AgNPs derived from the particle form or the released silver ions (Ag+). In this study, the toxic effects of two citrate-coated AgNPs (20 and 100 nm) and Ag+ were investigated in hepatoblastoma cells (HepG2 cells). The suppression tests showed that AgNPs and Ag+ induced cell apoptosis via different pathways, which led us to speculate on the AgNP-induced mitochondrial damage. Then, the mitochondrial damages induced by AgNPs and Ag+ were compared under the same intracellular Ag+ concentration, showing that the mitochondrial damage might be mainly attributed to Ag nanoparticles but not to Ag+. The interaction between AgNPs and mitochondria was analyzed using a scattered light imaging method combined with light intensity profiles and transmission electron microscopy. The colocalization of AgNPs and mitochondria was observed in both NP20- and NP100-treated HepG2 cells, indicating a potential direct interaction between AgNPs and mitochondria. These results together showed that AgNPs induced apoptosis in HepG2 cells through the particle-specific effects on mitochondria.